Product nameAnti-L1CAM antibody [UJ127.11]
See all L1CAM primary antibodies
DescriptionMouse monoclonal [UJ127.11] to L1CAM
SpecificityUJ127.11 may be useful in the diagnosis of embryonic tumours (e.g. neuroblastoma).
Tested applicationsSuitable for: WB, IP, IHC-Pmore details
Species reactivityReacts with: Human
Tissue, cells or virus corresponding to Human L1CAM. Homogenous suspension of 16 week human foetal brain.
Database link: P32004
General notesL1CAM can be detected between 200-220 kD. In brain samples it is typically seen at ~ 200 kD. When the protein is overexpressed in vitro it is often detected as a doublet with bands at 200 and 220 kD. The unglycosylated, unprocessed L1CAM is ~ 140-150 kDa. The protein has 21 putative N-glycosylation sites on the extracellular portion of the protein which, when they are all glycosylated, results in a detected MW of 200-220 kD depending upon how many residues are actually glycosylated. L1CAM can be cleaved by the metalloprotease ADAM10 resulting in fragments of 180 kD and 40 kD. L1CAM can also be cleaved by plasmin resulting in fragments of 140 kD and 80 kD. In theory, therefore, one could detect bands at ~220, 200, 180, 140, 80 and 40 kD.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Storage bufferConstituent: PBS
Concentration information loading...
PurityProtein A/G purified
Light chain typeunknown
Our Abpromise guarantee covers the use of ab20148 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use at an assay dependent concentration. Predicted molecular weight: 200-220 kDa. It may also detect smaller cleavage fragments (please see Notes below).|
|IP||Use at an assay dependent concentration.|
|IHC-P||Use at an assay dependent concentration.|
FunctionCell adhesion molecule with an important role in the development of the nervous system. Involved in neuron-neuron adhesion, neurite fasciculation, outgrowth of neurites, etc. Binds to axonin on neurons.
Involvement in diseaseDefects in L1CAM are the cause of hydrocephalus due to stenosis of the aqueduct of Sylvius (HSAS) [MIM:307000]. Hydrocephalus is a condition in which abnormal accumulation of cerebrospinal fluid in the brain causes increased intracranial pressure inside the skull. This is usually due to blockage of cerebrospinal fluid outflow in the brain ventricles or in the subarachnoid space at the base of the brain. In children is typically characterized by enlargement of the head, prominence of the forehead, brain atrophy, mental deterioration, and convulsions. In adults the syndrome includes incontinence, imbalance, and dementia. HSAS is characterized by mental retardation and enlarged brain ventricles.
Defects in L1CAM are the cause of mental retardation-aphasia-shuffling gait-adducted thumbs syndrome (MASA) [MIM:303350]; also known as corpus callosum hypoplasia, psychomotor retardation, adducted thumbs, spastic paraparesis, and hydrocephalus or CRASH syndrome. MASA is an X-linked recessive syndrome with a highly variable clinical spectrum. Main clinical features include spasticity and hyperreflexia of lower limbs, shuffling gait, mental retardation, aphasia and adducted thumbs. The features of spasticity have been referred to as complicated spastic paraplegia type 1 (SPG1). Some patients manifest corpus callosum hypoplasia and hydrocephalus. Inter- and intrafamilial variability is very wide, such that patients with hydrocephalus, MASA, SPG1, and agenesis of corpus callosum can be present within the same family.
Defects in L1CAM are the cause of spastic paraplegia X-linked type 1 (SPG1) [MIM:303350]. Spastic paraplegia is a degenerative spinal cord disorder characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs.
Note=Defects in L1CAM may contribute to Hirschsprung disease by modifying the effects of Hirschsprung disease-associated genes to cause intestinal aganglionosis.
Defects in L1CAM are a cause of partial agenesis of the corpus callosum (ACCPX) [MIM:304100]. A syndrome characterized by partial corpus callosum agenesis, hypoplasia of inferior vermis and cerebellum, mental retardation, seizures and spasticity. Other features include microcephaly, unusual facies, and Hirschsprung disease in some patients.
Sequence similaritiesBelongs to the immunoglobulin superfamily. L1/neurofascin/NgCAM family.
Contains 5 fibronectin type-III domains.
Contains 6 Ig-like C2-type (immunoglobulin-like) domains.
Cellular localizationCell membrane.
- Information by UniProt
- Antigen identified by monoclonal antibody R1 antibody
- CAML1 antibody
- CD171 antibody
Ab20148 Immunoprecipitating L1CAM in human Melanoma whole cell lysate. 1000 µg of cell lysate was incubated with primary antibody (5 µg/mg lysate, ab20148) and matrix (Protein G) for 12 hours at 4°C. For western blotting ab20148 (1/5000) was used to confirm successful immunoprecipitation.
Anti-L1CAM antibody [UJ127.11] (ab20148) at 5 µg/ml + SK N BE (Human neuroblastoma) Whole Cell Lysate at 10 µg
Goat polyclonal to Mouse IgG - H&L - Pre-Adsorbed (HRP at 1/3000 dilution
Predicted band size: 200-220 kDa
Observed band size: 200-220 kDa
This product has been referenced in:
- Zaatiti H et al. Tumorigenic proteins upregulated in the MYCN-amplified IMR-32 human neuroblastoma cells promote proliferation and migration. Int J Oncol 52:787-803 (2018). Read more (PubMed: 29328367) »
- Wang H et al. Plasma a-synuclein and cognitive impairment in the Parkinson's Associated Risk Syndrome: A pilot study. Neurobiol Dis 116:53-59 (2018). Read more (PubMed: 29705185) »